Asthma is a significant health burden ($12.76 in 1998) that disproportionately affects individuals of African descent, especially children, in degree of severity, steroid dependency, ER visits, hospitalizations, and deaths. Although ethnic minority group (EMG) status, low socioeconomic status, and residence in urban areas are closely linked in the US, few asthma genetic studies have included EMGs adequately defined by residence, self designated ancestry, and country of origin. The overall goal of this proposal is to distinguish the genetic basis of differences in asthma susceptibility and the course of asthma (e.g., risk of exacerbations) between African American (AA) and Caucasian (CA) populations through five Specific Aims: 1) Determine if the differences found in the expression of the "immortalization" pathway between the HapMap Project's Utah residents of European descent (CEU) and Yorubans in Nigeria (YRI) can be reproduced in AA and CA lymphoblast cells and to see if the set of genes differentially expressed is reproduced in small populations of AA and CA asthmatic children. These results will help to identify asthma risk gene variants and how their expression changes by race, environmental exposure and continent of origin (C01). 2) Create a web accessible public database from data extracted from databases at the NCBI and the N1EH combined with annotations mined from the literature. The result will be a race/ethnicity specific database of SNP distributions and mRNA expression changes of asthma environmental responsive genes by susceptibility and severity (REDSMAG). This database will provide researchers with access to a "one-stop" resource for asthma related gene variants with annotations as to how they inform risks and disease course in AA and CA. 3) Create co-morbidity model of asthma severity, co-morbidity, and demographic data extracted from medical records of heterogeneous AAs and CAs to allow comparison of the differences in these co-morbidity relationships when genomic data are added to the models in Aim 4. 4) Model asthma risk and exacerbation using combined clinical and genomic (SNP) data from the Childhood Asthma Management Project (CAMP) and compare those across AAs and CAs to identify pathways that are differentially expressed. 5) Expand race-ethnicity specific asthma study to a broader geographical area and other genome-scale modalities. (End of Abstract)